“…Actually, the antioxidant system has a primary responsibility in the defence against ROS. Normal injury increases portal and systemic endotoxin levels as well as translocation to the liver, which consequently causes neutrophils recruitment and the further release of ROS [48,49,50]. The formation and eradication of ROS in healthy cells are maintained by a radical scavenging system containing catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) [51].…”
In this study, we aimed to investigate the effects of p-Coumaric acid (PCA) on cisplatin (CIS)-induced hepatotoxicity and nephrotoxicity in Wistar adult rats for 24 h compared to untreated control groups. In this experiment, 40 Wistar adult rats were utilized and divided randomly into five groups. After 24 h of CIS administration, liver and kidneys were harvested and assessed by H&E staining. Also, markers for oxidative stress and antioxidants were analyzed in theses tissues. Compared to the control group, accumulation of malondialdehyde was increased in groups treated CIS, whereas superoxide dismutase activities and glutathione levels were distinctly diminished in this group. The study’s histopathological findings such as hydropic degeneration, vascular congestion, sinusoidal dilatation in hepatocytes and tubular necrosis in kidneys were in accordance with the results of markers for oxidative stress. PCA may prevent hepatotoxicity and nephrotoxicity by increased antioxidant enzymes and reduced oxidant parameters.
“…Actually, the antioxidant system has a primary responsibility in the defence against ROS. Normal injury increases portal and systemic endotoxin levels as well as translocation to the liver, which consequently causes neutrophils recruitment and the further release of ROS [48,49,50]. The formation and eradication of ROS in healthy cells are maintained by a radical scavenging system containing catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) [51].…”
In this study, we aimed to investigate the effects of p-Coumaric acid (PCA) on cisplatin (CIS)-induced hepatotoxicity and nephrotoxicity in Wistar adult rats for 24 h compared to untreated control groups. In this experiment, 40 Wistar adult rats were utilized and divided randomly into five groups. After 24 h of CIS administration, liver and kidneys were harvested and assessed by H&E staining. Also, markers for oxidative stress and antioxidants were analyzed in theses tissues. Compared to the control group, accumulation of malondialdehyde was increased in groups treated CIS, whereas superoxide dismutase activities and glutathione levels were distinctly diminished in this group. The study’s histopathological findings such as hydropic degeneration, vascular congestion, sinusoidal dilatation in hepatocytes and tubular necrosis in kidneys were in accordance with the results of markers for oxidative stress. PCA may prevent hepatotoxicity and nephrotoxicity by increased antioxidant enzymes and reduced oxidant parameters.
“…Ren et al 19 showed that 90% but not 70% hepatectomy increased portal and systemic endotoxin levels. After this observation, they used selective bowel decontam ination with gentamicin and showed that this reduced lipopolysaccharide levels, enhanced liver regeneration and increased the survival following 90% hepatectomy from 24% to 56% 19 . Given that sepsis due to gutrelated microorganisms is a major cause of death after major hepatic resection 20 , this finding is potentially important.…”
Although the normal liver has a fantastic regenerative capacity, following acute injury or resection this regener ative ability becomes overwhelmed in two important scenarios: in the setting of severe acute liver injury or when there is severe chronic liver injury with aberrant liver architecture and marked liver fibrosis 1,2 . These scenarios are clinically relevant and often result in serious morbidity and mortality 3 . While there have been decades of excellent and clinically informative research into understanding the signals that control regener ation of the normal liver 4 , the mechanisms at play when the abnor mal liver attempts regeneration are less well described 5 . Understanding how regeneration fails or is impaired in the severely damaged liver is an important goal. Lessons learned from relevant animal models might have impor tance in the clinical setting and aid the develop ment of new therapies to either promote regener ation or prevent complications that arise during the period of liver regeneration.A clinical scenario in which an improved understand ing of regeneration of the compromised liver would be of benefit includes liver transplantation, here the increas ingly common use of partial liver grafts such as split livers and living donor transplants relies upon regener ation of the donor graft to reach the correct liver mass 6 .Failure of regeneration in these settings results in poor or delayed graft function, prolonged intensive care stays, occasionally a requirement for retransplantation or, ulti mately, even death of the recipient 7,8 . By understanding the pathological mechanisms driving these adverse con ditions it is hoped that the period of regeneration can be more predictable and the associated clinical complications ultimately preventable. The ability to predict or improve liver regeneration when the liver is compromised -for example, in the setting of cirrhosis when surgical resection of hepatocellular cancer (HCC) is commonly performed, or following the resection of colorectal hepatic metastasis, when the liver has received prior chemotherapy -would enable clinicians to optimize cancer resection approaches. Furthermore, by understanding the mechanisms under lying normal liver regeneration and aberrant liver regener ation in chronic liver injury it is hoped that we will be able to promote 'healthy regeneration' or remodel ling in chronic liver disease. Such a scenario in which this approach could be applied includes liver cirrhosis. Here, the initial insult (such as viral hepatitis or autoimmune hepatitis) can sometimes be directly treated, but the liver tissue is left severely damaged and still susceptible to the clinical consequences of liver failure, portal hypertension and an increased risk of HCC 9 .Abstract | Liver regeneration has been studied for many decades and the mechanisms underlying regeneration of the normal liver following resection or moderate damage are well described. A large number of factors extrinsic (such as bile acids and circulating growth factors) and intrinsi...
“…Multiple human studies focused on either pre-or postresectional antibiotic prophylaxis, without evidence for a significant effect on the rate of infectious complications [147,148]. Preoperative selective bowel contamination has been explored in rodent models, showing amelioration of parenchymal injury and increased liver regeneration after partial liver resection [149]. A meta-analysis of human transplant studies however showed no benefits on infectious complications [150].…”
Liver failure is the main cause of death after partial liver resection for cancer, and is presumably caused by an insufficient quantity and function of the liver remnant. Detection of liver failure is often too late, and current treatment focuses on relieve of symptoms. New research initiatives explore artificial support of liver function and stimulation of regrowth of the remnant liver.
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